uPAR: An Essential Factor for Tumor Development

Lv, Tao; Zhao, Ying; Jiang, Xinni; Yuan, Hemei; Wang, Haibo; Cui, Xuelin; Xu, Jiashun; Zhao, Jingye; Wang, Jianlin

doi:10.7150/jca.62281

Cited by 24 publications

(20 citation statements)

References 182 publications

(230 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Based on these observations, it may be speculated that KLF4 may play a double role in the maintenance of the QCCs pool by maintaining a stemness state and restraining proliferation at the same time. In addition to KLF4, lung QCCs were characterized by an increased expression of urokinase plasminogen activator surface receptor (uPAR), a component of the plasminogen activation system involved in tumorigenesis, metastasis, EMT and chemoresistance [ 53 ], and by the two stemness-associated surface markers CD44 and CD166. Similarly, colorectal QCCs showed an increased expression of factors involved in stemness and self-renewal such as AXIN2, LGR5 and BMI1.…”

Section: Discussionmentioning

confidence: 99%

Analysis of Dormancy-Associated Transcriptional Networks Reveals a Shared Quiescence Signature in Lung and Colorectal Cancer

Cuccu

Francescangeli

Angelis

et al. 2022

IJMS

View full text Add to dashboard Cite

Quiescent cancer cells (QCCs) are a common feature of solid tumors, representing a major obstacle to the long-term success of cancer therapies. We isolated QCCs ex vivo from non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) xenografts with a label-retaining strategy and compared QCCs gene expression profiles to identify a shared “quiescence signature”. Principal Component Analysis (PCA) revealed a specific component neatly discriminating quiescent and replicative phenotypes in NSCLC and CRC. The discriminating component showed significant overlapping, with 688 genes in common including ZEB2, a master regulator of stem cell plasticity and epithelial-to-mesenchymal transition (EMT). Gene set enrichment analysis showed that QCCs of both NSCLC and CRC had an increased expression of factors related to stemness/self renewal, EMT, TGF-β, morphogenesis, cell adhesion and chemotaxis, whereas proliferating cells overexpressed Myc targets and factors involved in RNA metabolism. Eventually, we analyzed in depth by means of a complex network approach, both the ‘morphogenesis module’ and the subset of differentially expressed genes shared by NCSLC and CRC. This allowed us to recognize different gene regulation network wiring for quiescent and proliferating cells and to underpin few genes central for network integration that may represent new therapeutic vulnerabilities. Altogether, our results highlight common regulatory pathways in QCCs of lung and colorectal tumors that may be the target of future therapeutic interventions.

show abstract

Section: Discussionmentioning

confidence: 99%

Analysis of Dormancy-Associated Transcriptional Networks Reveals a Shared Quiescence Signature in Lung and Colorectal Cancer

Cuccu

Francescangeli

Angelis

et al. 2022

IJMS

View full text Add to dashboard Cite

show abstract

“…Circ_0003340 has previously been shown to be dysregulated in ESCC and facilitated ESCC cell proliferation, migration and invasion, and arrested apoptosis 25 . Angiogenesis is an important basis for tumor cell proliferation and metastasis, and the development of antiangiogenic drugs has become a hot spot in cancer research 26 . Our study identified a high abundance of circ_0003340 in ESCC, and found that knockdown of circ_0003340 notably restrained ESCC cell proliferation, migration, invasion and tube formation, but enhanced apoptosis.…”

Section: Discussionmentioning

confidence: 53%

“… 25 Angiogenesis is an important basis for tumor cell proliferation and metastasis, and the development of antiangiogenic drugs has become a hot spot in cancer research. 26 Our study identified a high abundance of circ_0003340 in ESCC, and found that knockdown of circ_0003340 notably restrained ESCC cell proliferation, migration, invasion and tube formation, but enhanced apoptosis. Moreover, circ_0003340 silencing also curbed tumor growth in vivo.…”

Section: Discussionmentioning

confidence: 58%

Circ_0003340 downregulation mitigates esophageal squamous cell carcinoma progression by targeting miR‐940/PRKAA1 axis

Guan

Wang

et al. 2022

Thoracic Cancer

View full text Add to dashboard Cite

Background Esophageal squamous cell carcinoma (ESCC) is a highly prevalent type of esophageal cancer (EC), usually found at an advanced stage with a high mortality rate, and it is now crucial to find new ways to diagnose and treat ESCC. This study analyzed the function of circular RNA_0003340 (circ_0003340)/microRNA‐940 (miR‐940)/protein kinase AMP‐activated alpha 1 catalytic subunit (PRKAA1) axis in ESCC. Methods Circ_0003340, miR‐940 and PRKAA1 contents were measured with the application of real‐time quantitative polymerase chain reaction (RT‐qPCR) and western blot. Cell proliferation, cell cycle, apoptosis, migration, invasion and angiogenesis were assessed with a cell counting kit‐8 (CCK8), 5‐ethynyl‐2′‐deoxyuridine (EdU), flow cytometry, wound healing, transwell and tube formation assays. We used both the luciferase reporter system and RNA immunoprecipitation (RIP) to analyze the relationship between miR‐940 and circ_0003340 or PRKAA1. Finally, xenograft models were applied to analyze the effect of circ_0003340 on tumor growth in vivo. Results Upregulated circ_0003340 and PRKAA1, and downregulated miR‐940 levels were detected in ESCC. Meanwhile, ESCC progression was apparently restrained by circ_0003340 knockdown in vitro. Circ_0003340 acted as a ceRNA for miR‐940 in regulating ESCC progression and miR‐940 was proved to target PRKAA1 to arrest ESCC progression in vitro. Finally, in vivo experiments established that silencing of circ_0003340 slowed tumor growth in vivo. Conclusion Circ_0003340 downregulation mitigated esophageal squamous cell carcinoma progression by targeting miR‐940/PRKAA1 axis.

show abstract

“…uPAR is a highly glycosylated protein that is anchored on the cell membrane surface in the form of glycosylphosphatidylinositol (GPI). [19][20][21] uPAR/uPA is involved in the progression of glioma, including tumorigenesis, cell proliferation, cell migration, adhesion, tumor invasion, and other pathological processes. [22][23][24] Downregulation of uPAR expression by small…”

Section: Discussionmentioning

confidence: 99%

A New Urokinase Plasminogen Activator Receptor‐Targeted Near‐Infrared Fluorescence (NIR) Probe for Glioma Imaging

Han

Zhang

et al. 2023

ChemistrySelect

View full text Add to dashboard Cite

A new fluorescent imaging probe indocyanine green‐VC (ICG‐VC) in the second near‐infrared window (NIR‐II) was fabricated based on the urokinase‐type plasminogen activator receptor (uPAR) targeted polypeptide VC (VSNKYFSNIHWGC). The relative quantum yield (ΦF)was 0.34 %. The tail of its fluorescence emission wavelength exceeded 1000 nm with excellent photostability. In vitro cell analysis, MTT results indicated the high biocompatibility of ICG‐VC with U87MG cells. ICG‐VC showed good photothermal conversion behavior and photothermal stability.In vivo NIR‐II fluorescence imaging, ICG‐VC exhibited high spatiotemporal resolution in the lymphatic vessels with a high resolution of 717 μm and signal‐to‐noise ratio of 4.36, and displayed an excellent U87MG tumor uptake within 4 h, which reached the maximum at 8 h with a signal‐to‐noise ratio of 5.32.

show abstract

uPAR: An Essential Factor for Tumor Development

Cited by 24 publications

References 182 publications

Analysis of Dormancy-Associated Transcriptional Networks Reveals a Shared Quiescence Signature in Lung and Colorectal Cancer

Analysis of Dormancy-Associated Transcriptional Networks Reveals a Shared Quiescence Signature in Lung and Colorectal Cancer

Circ_0003340 downregulation mitigates esophageal squamous cell carcinoma progression by targeting miR‐940/PRKAA1 axis

A New Urokinase Plasminogen Activator Receptor‐Targeted Near‐Infrared Fluorescence (NIR) Probe for Glioma Imaging

Contact Info

Product

Resources

About